etal lesion - Europe PMC

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Apr 10, 1988 - deficits or lateral homonymous hemianopia. On the other hand, there he had ... effectively treated simply by increasing the. BDZ dose. We haveĀ ...
1008 Lows of unilateral eye closure and right pan- able to maintain his eyes closed in a normal etal lesion way. He now complained, however, being unable to hunt (his favourite hobby) because Sir: Cases of inability to close the eyes vol- he was unable to aim with either eye. The untarily (apraxia of eye closure') and cases patient was right-handed and he used his of inability to maintain the eyes closed (eye- right eye for aiming. Simultaneous closure lid motor impersistence2 3) are known. We of the two eyes, voluntarily or reflexly, was report a patient in whom the acquired possible but unilateral closure of only either inability to close the eyes affected alterna- the right or of the left eye was impossible; the two eyes closed simultaneously or tively either one or the other eye. A 70 year old man was investigated for remained open. The patient's previous pracepileptic Jacksonian seizures of the left tice of hunting established that he was able upper limb. The seizures began in the left to aim with either his right or his left eye eyelid and then spread to the entire left side before his illness and hence to close each eye of the body. A CT scan showed a right pari- independently. The only way the patient etal tumour (fig). The patient underwent could still hunt was to maintain his left eye operation and the tumour proved to be a hidden by a headband. Clinical examination glioblastoma. A month after surgery clinical was still completely normal without any examination revealed no motor or sensory facial palsy. deficits or lateral homonymous hemianopia. Classically cortical lesions are considered On the other hand, there he had a construc- to affect contralateral face movements, in tional apraxia and a mild left spatial hemi- particular mouth muscles and to a lesser neglect. A disorder of eyelid control was also extent orbicularis occuli. It is reported that noted. The patient was able to open and to each hemisphere controls the orbicularis close his eyes when requested but when occuli muscles of both sides, with a contraasked to keep his eyes closed any attempt to lateral predominance.4 This anatomical communicate or any mental effort such as organisation explains eyelid motor impercalculating was accompanied by instanta- sistence in patients with a unilateral lesion. neous opening of the two eyes, in spite of In our patient the unilateral lesion also repeated orders by the examiner. Often, the caused a bilateral eyelid dysfunction and an left eye opened first, followed after a few sec- inability to close separately either the right onds by the right one. If the patient was or the left eye. This phenomenon was not a asked again to close his eyes, he did it easily, minor form of paralysis: all the eyelid movebut any attempt at verbal contact resulted in ments were completely normal when bithe re-opening of the two eyes, simulta- lateral and conjugate. The face movements also were normal (reflex, automatic and volneously or with the left one first. A month later the constructional apraxia untary). The disorder was solely an inability and neglect disappeared and the patient was to dissociate the two eyelid movements. We believe that this phenomenon is an apraxic disorder: a unilateral eyelid closure apraxia. The eyelid signs of our patient were of two types: at first there was a motor eyelid impersistence, followed 2 months later by a unilateral eyelid closure apraxia. Perhaps, these should be seen as two stages of the same syndrome. CATHERINE BELIN

JACQUES LARMANDE BERTRAND GAYMARD PIERRE LARMANDE

Department of Neurology, CHU Bretonneau, 37044 Tours Cedex, France

References

Lewandowsy M. Ueber Apraxie des lid Schlusses. Neurol Centralblat 1907;26:720. 2 Berlin L. Compulsive eye opening and associated phenomena. Arch Neurol Psych 1955; 73:597-601. I

Fig CT scan showing the right parietal glioblastoma.

Letters 3 Fisher M. Left hemiplegia and motor impersistence. J Nerv Ment Dis 1956;123:201-18. 4 Penfield W, Rasmussen T. The Cerebral Cortex of Man. New York: MacMeillan, 1950.

Accepted

10 April 1988

Disappointing results of increasing benzodiazepine dose after the development of anti-

convlsant tolerance

Sir: For several years we have been studying benzodiazepine (BDZ) anticonvulsant tolerance in humans1 and in an animal model.2 3 Clinically, it seems a fairly widely held (although as yet undocumented) view that the development of such tolerance cannot be effectively treated simply by increasing the BDZ dose. We have attempted to investigate

this problem by examining data from a defined group of patients, suffering from complex partial and/or grand mal seizures, who had been in a preliminary evaluation of the anticonvulsant efficacy of N-desmethylclobazam (NDMC),3 the active metabolite of clobazam. All patients had been given both clobazam and NDMC on separate occasions and we documented every instance where the BDZ dose had been increased when relapse followed initial improvement. Clobazam, usually given 20 mg/day initially, was increased by 10 mg increments, but because NDMC was only available in 30 mg capsules the dose of this drug (ti - 46 h) was increased from 30 mg/day to 30 mg and 60 mg on alternate days. Our data (table) show that on only one of thirteen occasions did an increase in dose produce substantial (clinically relevant) improvement. In this instance the patient (No. 4) was given clobazam 20 mg/day for only 6 weeks before his dose increase and in view of his weight (85 kg), and hence relatively low dose (mg/kg), it seems possible that only a very limited degree of tolerance had developed during this time. Interestingly, animal studies in our laboratories suggest that in benzodiazepine tolerant mice the expected rightwards shift of the anticonvulsant dose response curve is accompanied by a considerable reduction in the maximum response (unpublished data). This finding, which is supported by similar observations on tolerance to the behavioural suppressant effects in rats,4 would appear to